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Wednesday, February 23, 2011

Turning a gigantic ship like the Titanic, under way with a full head of steam, is said to take a lot of time and miles of open sea. Turning the ship of state-guided nutrition guidelines is proving to be equally difficult and time consuming. However, I think that it has begun. The signs of it are subtle but unmistakable. The message is simple but vague: “diet and exercise.”

That is hopeful, to my way of thinking, because we are a nation of individuals with free will. We are not confined together on the deck of a ship. We are free to choose our own course. But, in the absence of the certain knowledge of our impending doom (metabolically speaking), combined with the lack of an assurance of the safety and efficacy in choosing an alternative course, we are reluctant to change. Most of us “go along for the ride,” blindly content to follow the course determined by our captains of public health and guided by the pursers of the processed food industry. We are marshaled by the stewards (the media) who serve us our daily reminders -- avoid saturated fats, now called solid fats, and dietary cholesterol -- and the clinicians who bus up after them all with myriad medications for our mounting medical maladies.

Never mind that this course was based on a hypothesis that was based on a flawed epidemiological study (of 6, later 7 nations out of 22) and that “Epidemiological studies can only go to prove that an agent could have caused, but not that it did cause, an effect in any particular case.” From the beginning, the dissenters never had a chance once the AHA got behind the hypothesis with public advertising (and a fundraising effort) promoting their “risk factors” for heart disease.

Never mind that the body synthesizes its own cholesterol just to compensate for the amount that we don’t eat. Cholesterol is essential for all animal life. It is the essential structural component of all cell membranes and it repairs damage from inflammation in our blood vessels. Did you know that the brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis. And, that human breast milk contains significant amounts of cholesterol? And that it is an important component in the manufacture of bile acids, steroid hormones, and fat soluble vitamins including Vitamins A, D, E and K. And that in 1997, Ancel Keys, the father (way back in 1953) of the Lipid Hypothesis, said: “There’s no connection whatsoever between cholesterol in food [that would be dietary cholesterol!] and cholesterol in blood.” Note: the parenthetical remark was added by me. For the source of this citation, as well as to view all the past installments in this series, visit the archives of this series at http://danbrown-thenutritiondebate.blogspot.com.

Never mind that the evidence supporting saturated fat in the diet has been convincingly documented; never mind that those pursuing low fat diets in The Framingham Study had a higher incidence of all cause mortality. And, never mind that after 40 years the director had to admit (July 1992, Archives of Internal Medicine): "In Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol.” This startling message has been drowned out by the drum-beat to lower cholesterol, especially LDL, from public health officials, the AHA, Big Pharma, industrial food processors and by the clinical practitioners who peddle their statins.

Never mind that… Well, you get the idea. If you are interested in reading the evidence-based science out there, there are plenty of books and blogs by qualified writers (not hacks on a rant like me) who look closely at the science. One of the best of course – is Gary Taubes’s “Good Calories – Bad Calories” (Knopf, 2007). His new, more “accessible” “Why We Get Fat: And What to Do About It” (Knopf, 2010) is an easy read. Another author whose writing I admire is Mary Enig, PhD. Her article, with Sally Fallon, “The Truth About Saturated Fats” is a must read for starters. Her book, “Know Your Fats,” is highly technical but definitive. Malcolm Kendrick’s “The Great Cholesterol Myth” and Uffe Rafnskov’s “Kolesterolmyten” (“The Cholesterol Myths”) deal very effectively with the dietary cholesterol issue.

Among my favorite blogs is PāNū, by Kurt G. Harris, M. D. His sub-title is “Paleolithic Nutrition – emulating the evolutionary metabolic milieu.” On the lighter side, Tom Naughton’s Big Fat Fiasco series on youtube.com is a scream.

These writers would create a food pyramid very different from the recently released HHS/USDA Guidelines. But the latest guidelines do show signs of change: the ship has begun to turn. You’ll see how in the next installment.

Wednesday, February 16, 2011

The emphasis in the previous installment was on the role of insulin as the transport vehicle for glucose in the bloodstream. Insulin has an equally important role in fat accumulation (synthesis and storage) which relates to obesity. Insulin must be in the bloodstream whenever there are elevated levels of glucose present. Insulin transports the glucose to the cells for energy, and at the same time acts to block the breakdown and entry of energy from stored fat into the bloodstream. The reason is this: The body prefers to burn glucose as a quick and readily available source of energy. So, if glucose energy is available, that is, if we can eat it (any/all sugars and starches), or the body can find it (glycogen) in storage, or synthesize it (by gluconeogenesis) in the liver, the body will do that. If there is energy available from any one of these sources, then there is no need for energy from fat. So, the fat stays locked up in storage, awaiting famine, as in Paleolithic times.

The fat in storage in our bodies, as well as the fat we eat, is in the form of triglyceride molecules. A triglyceride molecule is comprised of three fatty acid molecules linked to one glycerol molecule. The triglyceride molecule is too big to get into the blood stream intact. Lipolysis is the breakdown of fat molecules. When the protein lipase in the adipose tissue is activated by any of numerous hormones, the triglyceride molecule breaks down into its component parts and the fatty acids are released into the blood and are then available for cellular uptake. Ketone bodies, produced as a byproduct, and the glycerol molecule, are used for energy too. This process occurs at night during an overnight fast and is called ketosis.

So, to summarize and repeat: We can’t be a fat burner and a sugar burner at the same time. Our body prefers to burn sugar (glucose) and will do so as long as 1) we eat things that will break down into glucose (all sugars and all carbohydrate foods), or 2) we have glucose stored (as glycogen) in the liver and the muscles, or 3) the liver can make glucose from excess amino acids (stored in the liver) from eating too much protein. Since insulin must be present in the bloodstream to transport glucose to the cells for energy, so long as there is an elevated level of insulin in the bloodstream, the unneeded food energy from any of the excess fat or carbohydrates consumed (that cannot otherwise be stored in the liver and muscles) will be accumulated as body fat (by de novo lipogenesis), instead of broken down and burned for energy. That is why we get fat. We’re living on refined sugars and starches, and saving our fat (and accumulating more) for “hard times.”

This is particularly easy for us to do today - get fat – by eating a so-called “balanced” diet that is heavily skewed towards carbohydrates (see installment #2 at http://danbrown-thenutritiondebate.blogspot.com). And we’ve done this to avoid dietary fats, and particularly saturated fats and dietary cholesterol that we’ve been told erroneously are bad for us. The low fat diet was supposed to protect us from “killer diseases” like heart disease, stroke and cancer; today there is little evidence that it provides protection and mounting evidence that limiting fats in the diet may do more harm than good. Obesity is the precursor (but not necessarily a requisite) condition for Metabolic Syndrome and other Diseases of Civilization, including many cancers.

A couple of years ago a New York Times page -one story reported on a new treatment modality being recommended for patients presenting with hypertension, hypercholesterolemia, and Type 2 diabetes or prediabetes with obesity. The impetus for the new modality was the failure of clinicians to treat obesity effectively, and this was due, they said, to patient noncompliance! (not the wrong “prescription” of “diet and lifestyle changes,” meaning a restricted-calorie, balanced diet and more exercise.) The new paradigm they recommended was a “workaround” using just pharmacological solutions. High blood pressure and high cholesterol both respond to medications. And many more new medications are now available for Type 2 diabetes.

Unfortunately, this solution often results in the pre-diabetic developing full-blown Type 2 diabetes (25% within 3-5years) and the diabetic patient getting progressively worse until they become insulin dependent (multiple daily injections!) and eventually develop one of the complications or co-morbidities, from which they will most likely -- almost assuredly, die.

Gary Taubes’s new book, “How We Get Fat: And What to Do About It” (Knopf, 2010), offers a different approach. I can’t wait to see how well this more “accessible” book is received, both by the medical community and the lay public.

Tuesday, February 15, 2011

Why do we get fat? We eat too much and don’t exercise enough, you say. Well, if you do, you’ve got company; that’s the conventional wisdom. It was most recently reinforced by the release on 1/31/11 of the “revised” “Dietary Guidelines for Americans, 2010.” This was at a joint press conference held by the Secretaries of the USDA and the HHS, both former farm state governors. It also means that you probably haven’t read, or certainly haven’t accepted, the Alternative Interpretation of the Energy In – Energy Out formulation explained in Installment #5 in this series. (To see previously published installments, go to http://danbrown-thenutritiondebate.blogspot.com.) It flat-out refutes the Lipid Hypothesis.

Gary Taubes, in his serious and rather heavy read, “Good Calories – Bad Calories,” introduced in Installment #4, makes the case convincingly. In number 5 of his “certain conclusions” in the Epilogue of that book (p. 454), he states, “Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior” (emphasis added by me). The “obesity is a disorder of excess fat accumulation” is not a tautology; the operative word here is “disorder.” Why do we accumulate (synthesize and store) fat rather than break down and burn (catabolize and oxidize) the fat calories we eat? What drives our hunger to the point of eating too much and too often? The answer, according to Taubes, is carbohydrates.

All of Taubes’s ten “certain conclusions” merit rereading now and again (see Installment #4 in the archives), but his last two speak directly to these questions: 9) “By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be;” and 10) “By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.”

The mechanism at work here is the effect that all carbohydrates exert on the hormone insulin. That includes all sugars and all starches, regardless of their glycemic index or glycemic load. When carbs are eaten by a healthy person with normal glucose metabolism and regulation, in the initial response the enzyme amylase in saliva in the mouth triggers a quick burst of ready-made insulin previously produced by the pancreas. The digestive process continues in the stomach where acids assist in starting to break down all the sugars and starches. Then, in the small intestine, additional enzymatic action further breaks down the sugars and starches to simple glucose, which are then absorbed through the wall of the small intestine and into the bloodstream. In a healthy person, with normal insulin sensitivity and non-impaired glucose response, the additional insulin, produced by the pancreas in response to elevated glucose levels in the blood, slowly “mops up” the glucose (takes it to the muscles, etc.) over a one to two hour period and then, with glucose, declines in level in the blood.

Thus, the primary function of insulin -- glucose transport – has been fulfilled. Its function is only slightly, but significantly and progressively altered in a person with impaired glucose tolerance and/or insulin resistance. These impairments are the first signs, often undetected and overlooked, of the metabolic disorder called pre-diabetes.

Until recently, the fasting blood glucose test was the most common test for diagnosing pre-diabetes. The diagnosis was confirmed with a more difficult and expensive test, called the Impaired Glucose Tolerance Test (IGTT), which takes 2 to 4 hours, with blood drawn at half hour intervals. Within the last year, however, there has been a change in protocols, and now a test called the Hb A1c, or simply the A1c, is becoming the norm.

In addition, the diagnostic standard for Type 2 Diabetes Mellitus has been lowered, from 7.0 to 6.5, and to 6.0 for pre-diabetes. Some physicians set a much lower standard. Dr. Richard K. Bernstein, himself a Type 1 diabetic and a pioneer in blood test monitoring to achieve “normal” blood sugars, uses an A1c of 5.8 to diagnose full-blown Type 2 diabetes. None of these tests are perfect; the single best indication for an individual is a series of blood glucose checks after eating, that is, post-prandial. This can be done at home on your own schedule, no appointment required. Just eat to the meter.

In the next installment, we’ll examine the other major role of insulin: its regulatory role in fat metabolism. When the regulation of this hormone is out of balance, the result is fat synthesis and accumulation. We get fat. We’ll explain next.

Friday, February 4, 2011

What exactly is Metabolic Syndrome and how is it diagnosed? There are several definitions but most have five “risk factors” in common, with the first always being obesity. It is variously defined as “central obesity” (what I have coined “omental adiposity”), or a Body Mass Index (BMI) ≥30, or elevated waist circumference (men ≥40 inches, women ≥35 inches). The other four “risk factors” are elevated triglycerides (≥150mg/dl), reduced HDL, the “good” cholesterol (men ≤40mg/dl, women ≤50mg/dl), elevated blood pressure (≥130/85mm Hg, or use of medications for hypertension) and elevated fasting glucose (≥100 mg/dl, or use of medications for hyperglycemia).

Metabolic Syndrome is just one of a larger class of disorders that have become known as the Diseases of Civilization. Metabolic Syndrome, because it is increasingly affecting Westernized populations at younger and younger ages, especially in the last fifty years, is more closely identified with diet and lifestyle factors. Gary Taubes (of “Good Calories-Bad Calories” fame) and many others, including (most humbly) me, identify Metabolic Syndrome primarily, I would say exclusively, with diet alone. To support this assertion, let’s look at some statistics of how the Western, and specifically the American diet, has changed in modern times. Granted, these are also only associations -- not causal relationships – and so need to be closely examined.

Annual sugar consumption in the US is now in excess 160 pounds per capita, and most of that is triglyceride-raising high fructose corn syrup (HFCS). HFCS is 55% fructose and 45% glucose. It was first introduced into the food supply in 1978 and today is ubiquitous. Look for it on food labels, in soft drinks, and also in breads, cereals, breakfast bars, lunch meats, yogurts, soups and condiments, and avoid it like the plague. Americans consumed only about 100 pounds of sugar (sucrose) per person in 1920 and only about 15 pounds in 1830, most of it molasses, according to the Diet Heart Publishing timeline cited in Installment #3.

Older readers will remember Vitamin D rich lard, the rendered fat from pigs. It was once the #1 cooking fat with 70% of the market. Today, highly processed soybean oil has 70% of the market, and zero vitamin D. And, again as the Diet Heart Publishing timeline points out, “now the experts who told us not to eat lard are telling us we are deficient in Vitamin D!”

Per capita butter consumption in 1910 was 18 pounds. By 2000 it was less than 4 pounds. By 1957 margarine outsold butter for the first time. We gave up butter’s beneficial vitamin A for the excess, inflammation-inducing omega 6 fatty acids found in margarine, vegetable shortening and processed vegetable oils. Interestingly, as the trans fat dangers of margarine have become apparent, by 2005 butter had started to enjoy a comeback and for the first time was outselling margarine, again according to the Diet Heart Publishing timeline.

Finally, we Americans, for the last half century in particular, have been buying and eating more and more refined, highly processed carbohydrates, starches and sugars included as ingredients in the prepared foods that increasingly dominate the choices available to us. We choose them largely for convenience as we go about our busy lives. These daily dietary choices portend our own destruction, metabolically speaking. The Metabolic Syndrome is becoming, indeed has become, the American Disease of Civilization and it is associated with a long list of related conditions, known as co-morbidities.

Research has yet to firmly establish the causal relationship, but it is common for a patient with metabolic syndrome to progress to T2 diabetes and cardio vascular disease (CVD). In the United States, CVD is the leading cause of death among both men and women, and the presence of type 2 diabetes double the risk. In fact, over 50% of deaths in patients with type 2 diabetes are due to CVD. People with Metabolic Syndrome have a significantly greater risk of CVD, particularly men over age 45 and women over 55. These people also have a fivefold risk of developing type 2 diabetes.

Metabolic Syndrome, a growing and commonly silent condition, thus poses a significant public health threat. Left unchecked, it will have a staggering effect on healthcare in the United States in the years ahead. So, what can be done to check this “epidemic”? If overweight and obesity is the common risk factor, then we have to ask, why do we get fat?

Wednesday, February 2, 2011

The dreaded Diseases of Civilization were first referenced in Installment #1 in this series. (See previously published installments archived at http://danbrown-thenutritiondebate.blogspot.com.) We began on that track about 10,000 years ago with the advent of agriculture, marking the transition from the Paleolithic era to the Neolithic. The nomadic hunter-gatherer discovered he could lead a more stationary existence on a diet largely comprised of cereal grains. This was a major shift in the human dietary. In the latter half of the last century this shift greatly accelerated. Today, many believe that this shift alone accounts for the emergent patterns of illnesses and medical disorders with which we are now beset.

In modern times, epidemiologists, who by definition look for patterns of health and illness in populations, have examined this change and associated factors in myriad retrospective studies. They have observed the health and illnesses of populations exposed to the “Western diet” and compared them to peoples who have lived in relative isolation without exposure to the dietary of the industrialized world.

Epidemiology, however, can only go so far. These studies typically show correlations in similar populations and differences in dissimilar populations. As we’ve noted earlier, however, correlation does not imply causation. “Epidemiological studies can only go to prove that an agent could have caused, but not that it did cause, an effect in any particular case” (emphasis added by me), according to the Wikipedia entry.

Nevertheless, in the early 1950’s noted physiologist Ancel Keys proffered his Lipid Hypothesis, based on selected data from a 22 country epidemiological study. In his original Six Country Analysis (1953), and later the Seven Countries Study, launched in 1956 and first published in 1970, Keys’s hypothesis implicated dietary fat, particularly saturated fat and cholesterol, in heart disease. Acceptance of his hypothesis grew quickly and allowed others, like the American Heart Association, to make educated, informed assertions. This in turn led to the AHA’s now well-known “risk factors,” the McGovern Report’s “Dietary Goals” and the now infamous (to me) “Dietary Guidelines for Americans” (see Installments #2 & #3). The latest of these guidelines were due to be finalized by HHS/USDA in December 2010 as I wrote this.

All of these “prescriptions” dispensed to the consumer “with an interest in eating” were still, however, nothing more than simple hypotheses and assertions. Hypotheses must be tested and retested by randomized controlled trials to produce and independently reproduce similar outcomes, and if they don’t, they must be rejected as false. There have been many large, lengthy and costly trials such as the Framingham Heart Study. These studies have continuously been revised, updated and reinterpreted and their outcomes disputed. Along the way, many medical researchers have come increasingly to view with skepticism the Lipid Hypothesis and its resultant restrictions on consuming fats, particularly saturated fat and dietary cholesterol. Many in the medical and nutrition professions now view those recommendations as deeply flawed and based on inadequate scientific proof.

Conversely, other aspects of the so-called Western diet, and in particular the specific dietary recommendations I have previously referred to as the Standard American Diet (SAD), which is 60% carbohydrate, have increasingly come to infer a causal relationship with various diseases and metabolic disorders. Chief among these is the Metabolic Syndrome.

The Metabolic Syndrome is relatively new on the scene and was first recognized in 1988 when it was mysteriously named Syndrome X. The Metabolic Syndrome, again according to Wikipedia, “is a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes. It affects one in five people, and prevalence increases with age. Some studies estimate the prevalence in the USA to be up to 25% of the population.” A recent CNBC.com story from Reuters, posted on 11/23/10, is headlined, “Half of Americans Facing Diabetes by 2020.” The lead-in then clarifies the headline as follows: “More than half of Americans will have diabetes or be prediabetic by 2020…” That is a daunting (and expensive) prospect.

In the next installment we’ll learn the clinical definition of Metabolic Syndrome and how is it diagnosed.

About Me

I was diagnosed a Type 2 diabetic in 1986. I started a Very Low Carb diet (Atkins Induction) in 2002 to lose weight. I didn’t realize at the time that it would put my diabetes in clinical remission, or that I would be able to give up almost all of my oral diabetes meds. I also didn’t understand that, as I lost weight and continued to eat Very Low Carb, my blood lipids would dramatically improve (doubling my HDL and cutting my triglycerides by 2/3rds) and that my blood pressure would drop from 130/90 to 110/70 on the same meds.
Over the years I changed from Atkins to the Bernstein Diet (designed for diabetics) and, altogether lost 170 pounds. I later regained some and then lost some. As long as I eat Very Low Carb, I am not hungry and I have lots of energy. And I no longer have any of the indications of Metabolic Syndrome.
My goal, as long as I have excess body fat, is to remain continuously in a ketogenic state, both for blood glucose regulation and continued weight loss. I expect that this regimen will continue to provide the benefits of reduced systemic inflammation, improved blood lipids and lower blood pressure as well.